Although an association between chronic maternal alcoholism and a specific pattern of altered growth, morphogenesis and function in the offspring was made in 1973, little is known about the etiology and developmental pathogenesis of this disorder referred to as the Fetal Alcohol Syndrome. A mouse model for this condition recently developed by one of us will be utilized in order to gain further basic understanding regarding the following: the amount and duration of maternal alcohol ingestion necessary to result in offspring with the fetal alcohol syndrome; a critical period prior to and after which maternal alcohol ingestion might have no affect on the developing embryo or fetus; the total spectrum of this disorder; establishment of the minimum amount of time required between withdrawal from alcohol and the beginning of a pregnancy resulting in normal offspring. We will attempt to develop a rat model of the fetal alcohol syndrome and will utilize the rat in addition to the mouse model previously developed, to correlate increasing amount of maternal alcohol ingestion with severity of CNS malformation and subsequent behavioral abnormalities and intellectual deficits. Finally, we will attempt to develop a voluntary self-addicting strain of rats in order to see if their offspring also have an increased incidence of malformations. The studies herein described will hopefully lead toward better management of children already afflicted with this disorder and ultimately toward prevention.